The relatively rapid acquisition of resistance to cancer drugs remains a key obstacle to successful cancer therapy. Substantial efforts to elucidate the molecular basis for such drug resistance have revealed a variety of mechanisms, including drug efflux, acquisition of drug binding-deficient mutants of the target, engagement of alternative survival pathways, epigenetic alterations). Treatment of NSCLC patients harboring activating EGFR mutations with EGFR tyrosine kinase inhibitors results in anti-tumor responses to therapy, however patients ultimately progress on therapy due to the acquisition of drug resistance. Known mechanisms of resistance include secondary mutations in the EGFR gene (EGFRT790M) or MET gene amplification, however the underlying mechanism of resistance remains to be elucidated in ˜40-45% of cases. New treatment methods are needed to successfully address heterogeneity within cancer cell populations and the emergence of cancer cells resistant to drug treatments.